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Is H1N1 Swine Flu Really A
Virus...Or Is It A Bacteria?
By Lawrence Broxmeyer, MD
10-2-9

ABSTRACT

On June 3rd, 2009 in Global Research, a curious
article by F. William Engdahl appeared entitled "Sarkozy's Secret
Plan for Mandatory Swine Flu Vaccination". In it Engdahl plainly states
that " The only problem with the Swine Flu (H1N1) Vaccine, is that
to date, neither WHO nor the US Government's Center for Diseases Control
(CDC) have succeeded to isolate, photograph with an electron microscope,
or chemically classify the H1N1 Influenza A virus". Furthermore there
was no scientifically published evidence that French virologists have done
so either. Therefore, mentioned Engdahl, "To mandate a vaccination
for a putative (supposed or assumed to exist) disease that has never
been characterized is dubious to say the least."

Engdahl wasn't finished. "Even more bizarre is the
admission by the US Government's Food and Drug Administration, an agency
responsible for the health and safety of its citizens, that the 'test' approved
for premature release to test for H1N1 is not even a proven test. More
to the point", continues F. William Engdahl, "there is no forensic
evidence in any of the deaths reported to date that has been presented
that proves scientifically that any single death being attributed to H1N1
Swine Flu virus was indeed caused by such a virus."

Therefore, all that is H1N1 does not glitter, at least
with respect to the tireless efforts of Virologists, Epidemiologists and
Health Officials to stake claim that the current "flu-like illness"
pandemic is tied to "Influenza".

Both the World Health Organization (WHO) and the Centers
for Disease Control (CDC) are fully aware of a far more serious and ongoing
tuberculosis Pandemic in the world today. Yet they choose to downplay the
link, disregarding the similar flu-like symptoms tuberculosis often begins
with. Despite this, and with regards to the present TB Pandemic, WHO freely
admits that there were more than 9 million new cases of TB worldwide, and
approximately 1.8 million deaths from the disease in 2007, the most recent
year for which data are available. The World Health Organization estimates
that there are presently 13.7 million people living with TB. An infectious
disease, TB has been on the rise since the 1980s. About one-third of the
world's population, or two billion people, carry the TB bacteria.

The "H" and "N" of influenza sub-typing,
revolves around two glycoproteins called Hemagglutin (H) and Neuraminidase
(N), both of which can be, and are, associated with infectious diseases
such as the minuscule, viral forms of tuberculosis, a disease which ought
to be high on the differential diagnosis for 'flu-like illness' . Since
August, 2008, a Medline study in the Journal of Clinical Biochemistry showed
that sputum neuraminidase levels over 1.0 mU per mL were proven associated
with having tuberculosis in 92% of cases, previous to which bacteria closely
related to TB were shown, through crystallization, to produce the same
protein neuraminidase used to subtype 'Influenza'. Furthermore, as of 2006,
it has become obvious in Menozzi's study that similar to Influenza, Tuberculosis
not only uses Hemagglutin to attach to the lung's epithelial cells it invades,
but requires Hemagglutin for dissemination of the disease to the rest of
the body.

Khomenko's 1993 study showed that the explosive contagiousness
of just such influenza-like forms of tuberculosis are exactly the stuff
that previous epidemics and pandemics could have been made of. Khomenko
was cited by Nobel nominee Lida Mattman in her textbook prior to her untimely
death last year. That is exactly why, that in response to the present world
"flu" pandemic, Japan's Health Ministry's Tuberculosis Infection
Diseases Control Division deputy director Takeshi Enami went hand in hand
with Yoshio Nanba, director of The Office of Pandemic Influenza Preparedness
and Response, to attend a news conference in Tokyo on May 1, 2009.

AMERICA'S TAKE

But back in the US, the CDC and NIH seem to feel differently,
ignoring everything but "the virus". There was much the same
"Influenza" talk when in 1990, a new multi-drug-resistant (MDR)
tuberculosis outbreak took place in a large Miami municipal hospital. Soon
thereafter, similar outbreaks in three New York City hospitals left many
sufferers dying within weeks. By 1992, approximately two years later, drug-resistant
tuberculosis had spread to seventeen US states, with mini-epidemics in
Florida, Michigan, New York, California, Texas, Massachusetts, and Pennsylvania
and was reported, not by the American, but the international media, as
out of control. Viral forms of swine, avian and human TB can be transmitted
from one species to another. By 1993 the World Health Organization (WHO),
proclaimed tuberculosis a global health emergency. (1)

1918 AND TODAY

No one can deny the similarities between the onset of
the 1918 epidemic and that of today, yet a Press Release, issued on August
19, 2008, by the National Institute of Allergy and Infectious Diseases
(NIAID), contains a striking finding and conclusion: The 20 to 40 million
deaths worldwide from the great 1918 Influenza ("Flu") Pandemic
were NOT due to "flu" or a virus, but to pneumonia caused by
massive bacterial infection." (2) Subsequently, a study published
in JAMA by Talbot and Moore (3) in 2000 showed that Mexican immigrants
to the US have the highest case rates for tuberculosis among foreign born
persons. Mexico is the country where Swine Flu deaths were first documented.

The research of Lawrence Broxmeyer MD first proclaimed
(4) that the 1918 pandemic was due to bacteria, particularly mutant forms
of flu-like fowl, swine, bovine, and human tuberculosis (TB) bacteria htttp://drbroxmeyer.netfirms.com/001pdfBIRDFLUEDITORIALPUBLISHED.pdf These
forms of tuberculosis are often viral-like, mutate frequently, and can
"skip" from one species to another. Moreover the antibodies from
such viral TB forms react in the compliment fixation and later "viral"
assays.(5) They also grow on cultures which are supposed to grow only viruses.

In a supportive 16-page-paper which appeared in Population
and Development Review, University of California demographers Andrew Noymer
and Michael Garenne came up with convincing statistics showing that undetected
tuberculosis may have been the real killer in the 1918 flu epidemic. (6)

THE ROOTS OF HISTORY

Noymer's hypothesis stands sound against history. Few
flu "experts" are aware that in medical texts printed circa 1918
"Influenza" was attributed not to a virus but a bacteria called
Mycobacterium influenzae, discovered by Pfeiffer and Canon (7) in
1892......not exactly a coincidence since Richard Pfeiffer worked, at one
time, for Robert Koch, the discoverer of tuberculosis, a disease caused
by another bacillus called Mycobacterium tuberculosis. Both mycobacteria
stained best with carbol-fuchsin, a bacterial stain commonly used in the
staining of mycobacteria as it has an affinity for the mycolic acids found
in their cell walls. Mycobacteria such as tuberculosis are particularly
deadly because they share properties of the fungi ("myco-") as
well as bacteria. TB was, not all that long ago, referred to as "captain
of the men of death". And it never lost its potential to kill.

Mycobacterium influenzae was considered by most to be
the cause of Influenza until 1933. But there were serious diagnostic problems
with Mycobacterium influenza. Stengel and Fox warned about them in their
widely quoted W.B. Saunder's 1915 version of "A Textbook of Pathology".
Problems with identification revolved mainly in that although the bacterial
influenza occurred abundantly in the sputum of flu patients at first, it
decreased in quantity as the cases advanced. And when purulent expectoration
stopped, whether the disease was still active or not, Mycobacterium influenzae
"disappears entirely".(8)

In 1933 English physicians Wilson Smith, Christopher
H. Andrewes, and Patrick P. Laidlaw (9) removed secretions from the throat
of a humans with flu-like symptoms thought to have "influenza",
and then filtered out a suspected infectious agent, which by virtue of
the fact that it went through a filter was falsely proclaimed, from the
onset, to be "a virus". Injecting it into ferrets, the ferrets
then developed the same flu-like symptoms which Smith, Andrews and Laidlaw
summarily declared as "influenza". In addition Sir Christopher
Andrewes suggested, with the help of Burnet and Bang, that the term "myxovirus",
meaning "mucous virus", be incorporated into a family name for
the Influenzas. This, one imagines, was because the organism came from
mucous secretions.

But to government pathologist and pioneer physician/researcher
William M. Crofton, who by virtue of his office as County pathologist had
examined some of Laidlaw's human "Flu" samples, Laidlaw's entire
study was flawed. Crofton found Laidlaw's Flu samples to be laced with
the bacillus Mycobacteria influenzae, which by then had been renamed Haemophilus
Influenzae. To Crofton this bacilli was the common denominator for the
Pandemic of 1918 he had witnessed, although the bacteria could be accompanied
by an array of opportunistic organisms such as Staph and Strep. Crofton
publically and personally confronted and challenged Laidlaw to come to
his laboratory for the proof that his Influenza samples weren't viral.
Crofton was convinced by the confirmation of scientists like Calmette at
Pasteur regarding how certain forms of tuberculosis, appearing both minuscule
and viral, could pass through the smallest of filters. Crofton himself
then established that tuberculosis could disappear into tissues as viruses
did, and then go through filters which stopped cold even most of those
"now invariably called viral disease". "Surely, then",
Crofton concluded, "Tuberculosis has more right to be considered a
true virus than these."(10) So, at a time when viral forms of TB where
scantily being documented, Crofton struggled to link H. Flu with the TB
it so often infected in coordination with, as historical and political
momentum carried Laidlaw's study through for posterity. A great opportunity
was missed to correct the record.

Frank Macfarlane Burnet was the first to grow "Influenza"
in a laboratory setting; in 1940 he grew influenza in embryonated chicken
eggs, using the allantoic sac. He obviously considered such a technique
"Influenza" specific, never bothering to consider that such an
allantoic site might also be an excellent site for culturing the viral
or Cell-Wall-Deficient (CWD) forms of tuberculosis and the mycobacteria.
Viral TB, in fact grows there as early as 6 hours after introduction into
such a place in chicken embryos.(11)

Furthermore, some of the filamentous forms of tuberculosis
mentioned by Corper (12) appear similar to those attributed to ''Influenza''
by biochemist and Influenza guru Burnet. (13)

It wasn't because Burnet didn't know that bacteria could
assume viral forms. The first, and for a time the only virologist in Australia,
it was Burnet who discovered bacteria in viral forms of Q-fever (14). And
in that same paper, proclaiming Virology as an Independent Science , and
after admitting that viruses, including influenza, are composed of the
same sorts of material as bacteria, Burnet struggles to differentiate Influenza
by the fact that it ''probably has no DNA'' and was therefore exclusively
RNA. (Ibid.). But, according to Xalabardar, some cell-wall-deficient mycobacterial
forms also are exclusively RNA. Furthermore, points out Xalabarder, such
cell-wall-deficient tubercular forms are true antigens, all of which, similar
to Influenza, induce the production of specific antibodies detectable by
complement fixation tests, such as those originally used to detect Influenza.
(5)

CONCLUSION

In a landmark study (15), Dr. Robert Donaldson, working
out of the Pathological Society of Great Britain had ruled out that the
mycobacteria now referred to as H. Influenza by itself was behind 1918,
perhaps because of its disappearing nature. Yet at the same time he quickly
added that there wasn't "the slightest shred of evidence" that
the disease was due to a "virus" or influenza. Nor was Donaldson
ever able to refute Broxmeyer and Noymer's feelings that TB was behind
the many deaths in the pandemic, specifically because it is well known
that secondary bacterial infections, be they from opportunistic Haemophilus
influenza or any other common bacteria, are a common secondary manifestation
in TB-infected lungs. During the pandemic, one-third of patients who had
Haemophilus influenza were also found to have tuberculosis - keeping in
mind, as always, that many other cases with TB went undiagnosed.

In order to understand why we have this emphasis by those
virologists invested in a 'killer flu' in the US today, one must look back
historically at the science itself. Until the late 1940s influenza 'viruses'
were studied as infections, which, although filterable, were conceived
of as analogous to bacteria, a kind of ultra or viral-like bacteria. Not
to be deterred, and still seeing Influenza as a great opportunity for virology,
in 1941 virologist Hirst (16) claimed that influenza ''virus'' could agglutinate
(or clot) red blood cells of fowl and other animal species. Such a hemagglutinin
discovery, in turn, led to fast assays of what is thought to be Influenza.
The "H" in H1N1 comes to us through Hirst, who showed that ''virus''
particles first adsorbed to the red cells and, after a certain time, eluted
again as a result of what could be interpreted as an enzymatic reaction.
But 6 years later, Middlebrook and Dubos (17) made this seem nothing more
than a cheap hat trick by showing that similarly red blood cell agglutination
could be produced by sera from patients with tuberculosis. Takahashi and
Ono (18,19) reviewed similar red cell agglutination occurring in the presence
of tuberculous serums.

As Influenza historian van Helvoort (20) aptly pointed
out, indeed, in the 1930s and 1940s the concept of 'filterable viruses',
including Influenza, were subject to such criticism that Virology's very
foundations were threatened. Dogmatized statements like those coming from
pioneer virologist Andre Lwoff in 1957 : ''Viruses should be considered
as viruses because viruses are viruses'' (21) were totally unacceptable,
and did little to help the situation. So it was in 1952 that Cornelius
P. Rhoads, Director of Sloan-Kettering Institute for Cancer Research in
New York City, remarked in a conference introduction that the term ''viruses'',
such as that of Influenza, had achieved ''a high professional status with
doubtful credentials''. (22)

Perhaps in his authoritative text, The Pathogenesis of
Tuberculosis, Johns Hopkin's head of pathology, Arnold Rich summed things
up best:

"In relation to the question of the effect of influenza
upon tuberculosis, it should be pointed out that in many cases in which
pulmonary tuberculosis has been thought to have followed an attack of influenza
it is altogether probable that the supposed attack of influenza was, in
reality, a manifestation of an existing tuberculous infection; for tuberculoprotein,
whether absorbed from a spreading lesion or injected into the body, can
cause constitutional symptoms (fever, malaise, headache, joint pains, anorexia,
prostration) quite like those of influenza".(23)

As Professor Hans Rosling (http://www.youtube.com/watch?v=V8bUtbODV-Q) has
so aptly pointed out: during the initial 13 days that WHO started gaining
data on Swine Flu Deaths, April 24-May 06, 2009, 31 people died of Swine
Flu. 29 of these were in Mexico and 2 in the US. During this same 13 day
window, 63,000 people, around the world died of tuberculosis. (http://www.who.int/research/en).

What we have today, is a pandemic with "flu-like"
symptoms. And flu-like symptoms doesn't necessarily mean "Influenza"
is its underlying cause.

Readers interested in the subject of Influenza/TB can
also go to Dr. Ron Paul, MD's take at: http://informationclearinghouse.info/article22507.htm

Other relevant links include:also applicable to the current
Swine Flu epidemic include: http://www.frequencyfoundation.com/2009/07/bird-flu-influenza-and-1918-case-for.html

2. DM Morens et al. Predominant role of bacterial pneumonia
as a cause of death in pandemic influenza: Implications for pandemic influenza
preparedness. The Journal of Infectious Diseases DOI: 10.1086/591708 (2008).